Tachycardiac arrhythmias may be classified as tachycardias in the narrower sense, in which the affected chamber of the heart (ventricle or atrium) contracts in an orderly manner but at a high, physiologically inappropriate rate. In fibrillation, however, there is an unordered contraction of the respective chamber because of a recurring stimulus in which the particular chamber makes practically no further contribution toward pumping a volume of blood.
Tachycardias may also be differentiated according to their site of occurrence. Ventricular tachycardias (VT) originate in the ventricle, whereas supraventricular tachycardias (SVT) originate above the ventricle, e.g., in the atrium.
Implantable cardiac stimulators in the form of cardiac pacemakers or cardioverter/defibrillators are known in the art. Such cardiac simulators are usually connected to electrode lines, which have stimulation electrodes and optionally additional defibrillation electrodes in a chamber of the heart or in the immediate vicinity thereof. A cardiac pacemaker may deliver an electric stimulation pulse to the muscle tissue of a chamber of a heart via a stimulation electrode to thereby induce a stimulated contraction of the chamber of the heart if the stimulation pulse is of a sufficient intensity and the myocardial tissue (myocardium) is not at that moment in a refractory phase. To trigger a stimulated contraction of a heart chamber in this way, electrode lines with relatively small-area stimulation electrodes are usually used because to trigger a stimulated contraction of a heart chamber, it is sufficient if only a small portion of the myocardium of this chamber is initially stimulated. Such a stimulated contraction of a heart chamber is referred to within the context of this description as a “stimulated event.” If a natural contraction of the chamber occurs, it is referred within the context of this description as an “intrinsic” or “natural” action or event. A contraction of the right atrium of the heart, for example, is referred to as an atrial event, and may be a natural atrial event, or in the case of an atrial pacemaker, may be a stimulated atrial event. In the same sense, natural (intrinsic) and stimulated left-ventricular and right-ventricular events are differentiated.
Local stimulation of the myocardium propagates by stimulus conduction from the stimulation site in the myocardium and leads to depolarization of the muscle cells, and thus to contraction of the myocardium. After a short period of time, repolarization of the muscle cells occurs and thus a relaxation of the myocardium. During the depolarization phase, myocardial cells are not sensitive to stimulus, i.e., they are refractory. The electric potentials associated with depolarization and repolarization can be detected and their course over time can be analyzed in the form of an electrocardiogram.
Natural (intrinsic) events are detected by deriving the electric potentials of the myocardium of the respective heart chamber with the help of sensing electrodes, which are part of a corresponding electrode line. The sensing electrodes may also at the same time be the stimulation electrodes, and may ultimately be used alternately as stimulation electrodes and as sensing electrodes. An electrode pair, comprising a tip electrode and a ring electrode, is typically provided for this sensing, the tip electrode also serving as a stimulation electrode. A bipolar intracardiac electrocardiogram (IEGM) is obtained in this way. Sensing and stimulation in the ventricle are performed with the help of a ventricular electrode line, and similarly sensing and stimulation in the atrium (in the right atrium) are performed using an atrial electrode line, with the ventricular and atrial lines being connected separately to the respective cardiac stimulator. In addition, a left-ventricular electrode line may also be provided, typically protruding into the vicinity of the left ventricle through the coronary sinus and a lateral vein branching off from the former, and may have a small-area stimulation electrode and/or sensing electrode there.
During operation of the cardiac stimulator, the sensing electrodes are connected to corresponding sensing units, which are designed to analyze a respective electrocardiogram recorded by using a sensing electrode (and/or a pair of sensing electrodes). In particular, the sensing electrodes detect atrial and/or ventricular events, i.e., natural atrial or ventricular contractions. This is done, for example, by comparing threshold values, i.e., an intrinsic event is detected when a particular intracardiac electrocardiogram exceeds a suitable predefined threshold value.
The particular intrinsic atrial heart rate (atrial frequency) and/or ventricular heart rate (ventricular frequency) may be derived from the frequency at which atrial and/or ventricular events follow one another. Tachycardias, for example, can be detected in this way.
The ICDs currently available on the market offer a number of functions for termination of atrial arrhythmias, in particular atrial fibrillation, by cardioversion shocks that are delivered automatically. These cardioversion shocks are triggered repeatedly in response to detection of an atrial fibrillation. Here, the ventricular rhythm is evaluated only for more reliable synchronization of the shock.
All of the currently known devices deliver these cardioversion shocks either independently of the ventricular rhythm, or deliver no cardioversion shock when the ventricular frequency exceeds a programmable value. In many applications, atrial cardioversion is allowed only at certain times of the day or night and may first be delayed to give preference to a spontaneous termination, if necessary.
There is still no sufficiently specific algorithm for treatment of atrial fibrillation to permit adequate treatment of cardiac insufficiency patients with persistent atrial fibrillations. In these patients, atrial fibrillation always requires treatment when the atrial fibrillation is rapidly conducted into the ventricle. These patients lose the ventricular filling component due to an optimized AV time due to the atrial fibrillation. If the ventricular response exceeds a certain frequency, these patients also lose ventricular resynchronization, and with an increase in ventricular frequency, at the same time the cardiac output drops with an increase in myocardial oxygen demand. This leads to rapid decompensation in these patients. Immediate cardioversion of the atrial fibrillation is the only effective therapy here if the risk of thrombosis can be largely ruled out.